Control of TCF-4 Expression by VDR and Vitamin D in the Mouse Mammary Gland and Colorectal Cancer Cell Lines

Beildeck, Marcy E.; Islam,; Shah, Shilpan; Welsh, JoEllen; Byers, Stephen W.

doi:10.1371/journal.pone.0007872

Cited by 55 publications

(41 citation statements)

References 59 publications

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“…These findings indicate that the up-regulation of E-cadherin is just one of the mechanisms by which Vit D may negatively affect the b-catenin signaling pathway (Shah et al, 2006). These observations also indicate that the effects of 1,25(OH) 2 D 3 on the growth and differentiation of many different epithelial cancer cells may be, in part, explained by its ability to differentially regulate the activity of VDR, Ecadherin, and b-catenin/TCF pathways (Beildeck et al, 2009;Shah et al, 2006 …”

Section: Vit D Interaction With Wnt/b-catenin-signaling Pathwaysmentioning

confidence: 87%

Vitamin D in cancer chemoprevention

Giammanco¹,

Majo²,

Guardia

et al. 2015

Pharmaceutical Biology

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Context: There is increasing evidence that Vitamin D (Vit D) and its metabolites, besides their well-known calcium-related functions, may also exert antiproliferative, pro-differentiating, and immune modulatory effects on tumor cells in vitro and may also delay tumor growth in vivo. Objective: The aim of this review is to provide fresh insight into the most recent advances on the role of Vit D and its analogues as chemopreventive drugs in cancer therapy. Methods: A systematic review of experimental and clinical studies on Vit D and cancer was undertaken by using the major electronic health database including ISI Web of Science, Medline, PubMed, Scopus and Google Scholar. Results and conclusion: Experimental and clinical observations suggest that Vit D and its analogues may be effective in preventing the malignant transformation and/or the progression of various types of human tumors including breast cancer, prostate cancer, colorectal cancer, and some hematological malignances. These findings suggest the possibility of the clinical use of these molecules as novel potential chemopreventive and anticancer agents.

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Section: Vit D Interaction With Wnt/b-catenin-signaling Pathwaysmentioning

confidence: 87%

Vitamin D in cancer chemoprevention

Giammanco¹,

Majo²,

Guardia

et al. 2015

Pharmaceutical Biology

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“…Ca has been proposed to act through modification of cell signalling or in saponification of bile acids in the colon. Vitamin D is a nuclear receptor ligand that will modify apoptosis and mitosis through the RASmitogen-activated protein kinase and phosphoinositide 3-kinase pathways (92,(95)(96)(97) , and because of this may well interact with nutrients that affect overlapping pathways. However, the effect is likely to be complex as indicated by the observation that CRC is associated with overexpression of the vitamin D receptor (98) .…”

Section: Milk and Dairy Productsmentioning

confidence: 99%

Recent advances in understanding the role of diet and obesity in the development of colorectal cancer

et al. 2011

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Colorectal cancer (CRC) is a major cause of premature death in the UK and many developed countries. However, the risk of developing CRC is well recognised to be associated not only with diet but also with obesity and lack of exercise. While epidemiological evidence shows an association with factors such as high red meat intake and low intake of vegetables, fibre and fish, the mechanisms underlying these effects are only now being elucidated. CRC develops over many years and is typically characterised by an accumulation of mutations, which may arise as a consequence of inherited polymorphisms in key genes, but more commonly as a result of spontaneously arising mutations affecting genes controlling cell proliferation, differentiation, apoptosis and DNA repair. Epigenetic changes are observed throughout the progress from normal morphology through formation of adenoma, and the subsequent development of carcinoma. The reasons why this accumulation of loss of homoeostatic controls arises are unclear but chronic inflammation has been proposed to play a central role. Obesity is associated with increased plasma levels of chemokines and adipokines characteristic of chronic systemic inflammation, and dietary factors such as fish oils and phytochemicals have been shown to have anti-inflammatory properties as well as modulating established risk factors such as apoptosis and cell proliferation. There is also some evidence that diet can modify epigenetic changes. This paper briefly reviews the current state of knowledge in relation to CRC development and considers evidence for potential mechanisms by which diet may modify risk.

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“…The WNT signaling pathway regulates cell fate in a large number of developmental processes and differentiation during embryogenesis (7,8). In addition, the vital role of this pathway in tumorigenesis arouses great research interest (9)(10)(11).…”

Section: Introductionmentioning

confidence: 99%

SPINDLIN1 Promotes Cancer Cell Proliferation through Activation of WNT/TCF-4 Signaling

Wang¹,

Zeng²,

Chen³

et al. 2012

Molecular Cancer Research

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SPINDLIN1, a new member of the SPIN/SSTY gene family, was first identified as a gene highly expressed in ovarian cancer cells. We have previously shown that it is involved in the process of spindle organization and chromosomal stability and plays a role in the development of cancer. Nevertheless, the mechanisms underlying its oncogenic role are still largely unknown. Here, we first showed that expression of SPINDLIN1 is upregulated in clinical tumors. Ectopic expression of SPINDLIN1 promoted cancer cell proliferation and activated WNT/T-cell factor (TCF)-4 signaling. The Ser84 and Ser99 amino acids within SPINDLIN1 were further identified as the key functional sites in WNT/TCF-4 signaling activation. Mutation of these two sites of SPINDLIN1 abolished its effects on promoting WNT/TCF-4 signaling and cancer cell proliferation. We further found that Aurora-A could interact with and phosphorylate SPINDLIN1 at its key functional sites, Ser84 and Ser99, suggesting that phosphorylation of SPINDLIN1 is involved in its oncogenic function. Collectively, these results suggest that SPINDLIN1, which may be a novel substrate of the Aurora-A kinase, promotes cancer cell growth through WNT/ TCF-4 signaling activation. Mol Cancer Res; 10(3); 326-35. Ó2012 AACR.

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Control of TCF-4 Expression by VDR and Vitamin D in the Mouse Mammary Gland and Colorectal Cancer Cell Lines

Cited by 55 publications

References 59 publications

Vitamin D in cancer chemoprevention

Vitamin D in cancer chemoprevention

Recent advances in understanding the role of diet and obesity in the development of colorectal cancer

SPINDLIN1 Promotes Cancer Cell Proliferation through Activation of WNT/TCF-4 Signaling

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